Effect of posture on heart rate and cardiac axis of mice

Effect of change in body posture on cardiac electrical axis has not been well documented. Hence the present work was undertaken to study the effect of passive head-up and head-down postures on ventricular QRS axis and heart rate of anesthetised mice. During head-up posture, there was a statistically significant (P less than 0.02) increase in heart rate whereas during head-down posture, the heart rate decreased insignificantly. These changes in heart rate can be explained on the basis of synus and aortic nerve mediated baroreceptor reflexes. Ventricular QRS axis showed a significant increase (P less than 0.02) during head-up posture and an insignificant decrease during head-down posture. A change in the posture is likely to produce a change in anatomical orientation of heart within the thorax resulting in alteration of electrical axis of the heart.     

Effect of acebutolol, a new beta-receptor antagonist on heart rate and rate-pressure product in normal subjects.

A study on the effect of acebutolol, a new beta receptor antagonist, on the resting and post-exercise heart rate and rate-pressure product was carried out in 8 normal volunteers. Intravenous administration of 10 and 20 mg acebutolol was compared with 10 and 20 mg practolol administered at weekly intervals. In the oral study, increasing doses of acebutolol were administered over a period of 20 days. The heart rate and blood pressure was recorded before and at the completion of 4-minute exercise period. The exercise was carried out on a bicycle ergometer at 150 watt per minute for 4 minutes. In a dose to dose comparison, the potencies of acebutolol and practolol administered intravenously were of the same order, in decreasing the resting and post-exercise heart rate and rate pressure product. Their duration of action was also similar. In the oral study, the peak effect was achieved at a dosage of 200 mg per day (100 mg twice daily) of acebutolol. Acebutolol decreased the resting as well as post-exercise rate-pressure product (cardiac work load). This may be the mechanism for the reported beneficial effect in angina pectoris. Acebutolol was well tolerated and no serious side-effects were observed.     

Effect of two selected yogic breathing techniques of heart rate variability

The heart rate variability (HRV) is an indicator of the cardiac autonomic control. Two spectral components are usually recorded, viz. high frequency (0.15-0.50 Hz), which is due to vagal efferent activity and a low frequency component (0.05-0.15 Hz), due to sympathetic activity. The present study was conducted to study the HRV in two yoga practices which have been previously reported to have opposite effects, viz, sympathetic stimulation (kapalabhati, breathing at high frequency, i.e., 2.0 Hz) and reduced sympathetic activity (nadisuddhi, alternate nostril breathing). Twelve male volunteers (age range, 21 to 33 years) were assessed before and after each practice on separate days. The electrocardiogram (lead I) was digitized on-line and off-line analysis was done. The results showed a significant increase in low frequency (LF) power and LF/HF ratio while high frequency (HF) power was significantly lower following kapalabhati. There were no significant changes following nadisuddhi. The results suggest that kapalabhati modifies the autonomic status by increasing sympathetic activity with reduced vagal activity. The study also suggests that HRV is a more useful psychophysiological measure than heart rate alone.     

Effect of yoga on cardiovascular system in subjects above 40 years

This study was conducted to examine the effect of yoga on cardiovascular function in subjects above 40 yrs of age. Pulse rate, systolic and diastolic blood pressure and Valsalva ratio were studied in 50 control subjects (not doing any type of physical exercise) and 50 study subjects who had been practicing yoga for 5 years. From the study it was observed that significant reduction in the pulse rate occurs in subjects practicing yoga (P<0.001). The difference in the mean values of systolic and diastolic blood pressure between study group and control group was also statistically significant (P<0.01 and P<0.001 respectively). The systolic and diastolic blood pressure showed significant positive correlation with age in the study group (r1 systolic= 0.631 and r1 diastolic = 0.610) as well as in the control group (r2 systolic = 0.981 and r2 diastolic = 0.864). The significance of difference between correlation coefficient of both the groups was also tested with the use of Z transformation and the difference was significant (Z systolic= 4.041 and Z diastolic= 2.901). Valsalva ratio was also found to be significantly higher in yoga practitioners than in controls (P<0.001). Our results indicate that yoga reduces the age related deterioration in cardiovascular functions.     

Effect of yoga on exercise tolerance in normal healthy volunteers

Twelve normal healthy volunteers (6 males and 6 females) undergoing yoga training for 90 days were studied for the effect of yoga on exercise tolerance. Their ages ranged from 18 to 28 years. The volunteers were taught only Pranayama for the first 20 days and later on yogic asanas were added. Sub-maximal exercise tolerance test was done on a motorized treadmill by using Balke's modified protocol, initially, after 20 days (Phase-I) and after 90 days of yoga training (Phase-II). Pyruvate and lactate in venous blood and blood gases in capillary blood were estimated immediately before and after the exercise. Minute ventilation and oxygen consumption were estimated before and during the test. Post exercise blood lactate was elevated significantly during initial and Phase-I, but not in Phase-II. There was significant reduction of minute ventilation and oxygen consumption only in males in Phase-I and II at the time when the volunteers reached their 80% of the predicted heart rate. Female volunteers were able to go to higher loads of exercise in Phase-I and II.     

Effect of infused adenosine on cardiac output and systemic resistance in normal subjects.

1. The purine nucleoside adenosine relaxes smooth muscle in vitro and is a vasodilator in animals, but its effects on cardiac output and systemic vascular resistance have not been measured in normal conscious human subjects. 2. We have studied the effects of infused adenosine in doses of 0.005, 0.03 and 0.07 mg kg-1 min-1 on pulmonary blood flow and systemic vascular resistance in eight healthy volunteers, using a non-invasive, inert gas method and mass spectrometry. 3. At a dose of 0.07 mg kg-1 min-1, there was a rise in effective pulmonary blood flow (which is approximately equivalent to cardiac output) of 0.52 +/- 0.08 l min-1 m-2 (mean +/- s.e. mean) and a fall in estimated systemic vascular resistance of 357 +/- 44 dyn s cm-5. Despite this marked systemic vasodilation, there was no significant change in mean heart rate. 4. The effects of this dose of adenosine were maximal 2 min after starting the infusion, and had disappeared within 5 min of stopping it. 5. Adenosine may be therapeutically useful in the reduction of left ventricular afterload, where the absence of reflex tachycardia may be advantageous. We suggest that adenosine in doses of 0.03 mg kg-1 min-1 should be evaluated as a selective pulmonary vasodilator.     

心率控制对慢性心力衰竭患者心功能的影响

目的观察慢性心力衰竭患者入院后予以积极控制心率后对心功能的影响。方法选择2015年1月至12月在上海市浦东医院心血管内科住院纽约心脏学会(NYHA)心功能分级Ⅱ~Ⅳ级的120例充血性心力衰竭(CHF)患者,随机数字表法分配至治疗组及对照组,所有患者在常规治疗基础上,治疗组予以琥珀酸美托洛尔缓释片积极控制心率,以患者静息心率降至55~60次/min为目标心率指导药物治疗。检测2组治疗前、治疗12个月后静息心率,左室舒张末期内径(LVEDD),左室收缩末期内径(LVESD),左心室射血分数,6min步行试验距离以及血清脑钠肽(BNP)水平,以心力衰竭再入院为终点事件。结果治疗12个月后,治疗组患者静息心率显著低于对照组(P<0.01),治疗组患者LVEDD、LVESD及血浆BNP水平显著低于对照组,6min步行试验距离、LVEF显著高于对照组(P<0.05),心衰再入院率低于对照组(P<0.05)。结论积极控制心率可以改善CHF患者心功能。     

Valsalva constrictor and heart rate reflexes in subjects with essential hypertension and with normal blood pressure

1. The haemodynamic and heart rate responses to graded expiratory pressures were studied during Valsalva manoeuvres of standard 30 s duration in two groups of normotensives in the upper (n= 10) and lower (n= 9) halves of the ‘normal’ blood pressure range, and in a group of essential hypertensive subjects with minimal complications (n= 10). Haemodynamic variables were arterial, atrial and peripheral vein pressures, cardiac output and total peripheral resistance. 2. Reflex and mechanical effects of the manoeuvre were assessed in each subject from changes in the relationship between the expiratory pressure and circulatory responses before autonomic blockade, after cardiac effector block and after ‘total’ blockade. 3. The relationships between expiratory pressure and central and peripheral vein pressures were not changed by autonomic blockade, indicating that they depended on mechanical factors. In hypertensives the rise in venous pressures per unit expiratory pressure was significantly smaller than in normotensive subjects. 4. The expiratory pressure-related rise in total peripheral resistance was reflex and was similar in magnitude in all groups before autonomic blockade. However, after cardiac effector blockade the rise was greatest in the hypertensive subjects. The sensitivity of the constrictor response was related to the subjects’ resting total peripheral resistance index when measurements from all subjects were included. 5. The reflex heart rate responses of the hypertensives showed: (i) accentuation of the bradycardia at the start of forced expiration; (ii) an increased threshold for eliciting tachycardia during the latter part of the manoeuvre; and (iii) attenuation of the ‘overshoot’ bradycardia following release of expiratory pressure. 6. The differences between the responses of hypertensives and normotensives were relatively small and probably depended at least partly on differences in venous filling, structural differences of resistance vessels and different afferent inputs through arterial and cardiopulmonary baroreceptors.     

Comparison between the effects of inhaled isoprenaline and fenoterol on plasma cyclic AMP and heart rate in normal subjects

The time course of changes in plasma cyclic AMP, heart rate and bronchial tone after inhalation of fenoterol or isoprenaline from a dose-metered aerosol are reported in a group of normal subjects. After isoprenaline, plasma cyclic AMP increased rapidly reaching a peak by 10 min and returned to basal levels within 60 min. A rapid, transient rise in heart rate occurred that was maximal by 5 min and returned to a basal level by 45 min. After fenoterol, the changes in cyclic AMP and heart rate were of much longer duration. The rise in plasma cyclic AMP was slower in onset and of greater magnitude than for isoprenaline, reaching a peak by 20 min and remaining above basal level for more than 6 h. The maximum increase in heart rate after fenoterol was less than that observed with isoprenaline but an elevated rate persisted for 4 h after inhalation of fenoterol. Fenoterol is known to have a longer duration of action as a bronchodilator in comparison with isoprenaline. The prolonged rise in plasma cyclic AMP in normal subjects given inhaled fenoterol may reflect this long duration of action. The concomitant rise in heart rate, however, suggests that the duration of plasma cyclic AMP response may in part be due to the systemic effect of the fraction of inhaled fenoterol known to be absorbed via the buccal and intestinal routes.     

早孕期超声检查胎儿颈项透明层厚度 心率及心轴对胎儿先天性心脏病的预测价值

目的 探讨早孕期超声检查胎儿颈项透明层（NT）厚度、心率及心轴对胎儿先天性心脏病的预测价值。方法 选择2015年7月1日至2017年7月1日就诊于安徽医科大学第二附属医院的168例孕龄12～14周孕妇（均为单胎妊娠）,采用彩色多普勒超声测定胎儿NT、心率、心轴,所有孕妇均随访至分娩后1周,统计胎儿发生先天性心脏病的例数,绘制ROC曲线,分析NT厚度、心率及心轴对胎儿先天性心脏病的预测价值。结果 NT预测胎儿先天性心脏病ROC曲线下面积为0.895（P<0.001）,NT预测胎儿先天性心脏病最佳截点为2.995 mm,此时灵敏度为0.882,特异度为0.961;心轴预测胎儿先天性心脏病ROC曲线下面积为0.657（P=0.021）,心轴预测胎儿先天性心脏病最佳截点为50.891度,此时灵敏度为0.643,特异度为0.598;心率预测胎儿先天性心脏病ROC曲线下面积为0.616（P=0.045）,心率预测胎儿先天性心脏病最佳截点为179次/分钟,此时灵敏度为0.556,特异度为0.879。结论 孕早期NT厚度、心率及心轴检查对预测胎儿先天性心脏病及心脏畸形具有一定临床意义,其中NT厚度预测价值最大。     

Effect of cardiac vagal outflow on complexity and fractal correlation properties of heart rate dynamics

1. Cardiac vagal outflow is the major factor determining the magnitude of heart rate (HR) variability analysed by traditional time and frequency domain methods. New analysis techniques, such as fractal and complexity methods, have been developed to probe non-linear features in HR behaviour that may not be detectable by traditional methods. 2. We investigated the effects of vagal blockade (glycopyrrolate i.v. 5 microg kg-1 h-1 for 2 h, n = 8 vs. unmedicated control group, n = 8) and various breathing patterns (n = 12) on two non-linear measures of HR variability--detrended fluctuation analysis (DFA) and approximate entropy (ApEn)--in healthy male volunteers. 3. Glycopyrrolate decreased the mean (+/-SD) ApEn from 1.46 +/- 0.18 to 0.85 +/- 0.24 (P = 0.001 in comparison with the control group), and increased the short-term (alpha 1) and intermediate-term (alpha 2) fractal scaling exponents of DFA, alpha 1 from 0.96 +/- 0.19 to 1.43 +/- 0.29 (P = 0.003) and alpha 2 from 1.13 +/- 0.10 to 1.34 +/- 0.14 (P < 0.001). 4. Decrease in fixed respiration rate from 15 to 6 breaths min-1 increased alpha 1 from 0.83 +/- 0.25 to 1.18 +/- 0.27 (P < 0.001), but decreased alpha 2 from 0.88 +/- 0.09 to 0.45 +/- 0.17 (P < 0.001) and ApEn from 1.26 +/- 0.12 to 1.10 +/- 0.14 (P = 0.028). Rapid breathing (24 min-1) had no influence on these non-linear measures of HR variability. Hyperventilation (15 min-1, tidal volume increased voluntarily by 0.5 l) decreased alpha 1 from 0.83 +/- 0.25 to 0.66 +/- 0.28 (P = 0.002) but did not affect alpha 2 or ApEn. 5. To conclude, vagal blockade alters the fractal scaling properties of R-R intervals (alpha 1, alpha 2) and reduces the complexity (ApEn) of HR behaviour. Both the fractal and complexity measures of HR variability can also be influenced by changes in the breathing pattern.     

Effect of ICI 118551 on bronchial beta-adrenoceptor function and exercise heart rate in normal man.

To determine whether the beta 2-selectivity of ICI 118551 extended to human airways, we measured bronchial beta-adrenoceptor blockade and the reduction in exercise heart rate in six normal subjects on different occasions after ingestion of ICI 118551 20 or 50 mg, propranolol 40 mg or placebo in random order. Bronchial beta-adrenoceptor blockade after each active drug was measured as the displacement of the airway dose-response curve to salbutamol and expressed as a dose ratio. Exercise heart rate was measured during the fifth minute of steady state exercise at 70% of the subject's maximum work load. The mean dose ratios for the salbutamol airway dose-response curves following ICI 118551 20 and 50 mg and propranolol 40 mg were 11, 55 and 48 respectively. The mean reductions in exercise heart rate for the three drugs were 0.6, 6.6 and 16.6% respectively. These results confirm that the beta 2-selectivity of ICI 118551 includes airway beta 2-adrenoceptors in man.     

同型半脱氨酸水平不同的高血压病人静息心率及心率变异性分析

目的探讨H型高血压病人的静息心率及心率变异性的特点。方法 选择2017年1月1日至2017年12月31日安徽医科大学第二附属医院就诊的高血压病人141例,采用酶循环法测定其血液同型半胱氨酸(Hcy)浓度,借此分为A组(Hcy<10 μmol/L)20例、B组(10 μmol/L≤Hcy<15 μmol/L)69例和C组(Hcy>15 μmol/L)52例,记录各组常规心电图及动态心电图,比较各组静息心率及心率变异性的区别。结果(1)A、B、C组在静息心率(67.2±8.0)、(68.1±7.6)、(75.3±10.1)次/分、SDNN(123.9±37.6)、(117.6±29.9)、(94.7±27.6)ms、SDNN index(54.2±17.6)、(52.3±21.9)、(39.8±17.6)ms 、pNN50(12.9±10.3)%、(9.6±7.3)%、(5.6±6.8)%、HF(284.2±211.2)、(234.3±252.9)、(133.1±104.2)ms²及LF(387.0±209.8)、(343.6±187.8)、(212.3±180.0)ms²等指标间差异有统计学意义(P<0.05),但B组与A组之间差异无统计学意义(P>0.05),三组rMSSD(36.8±14.5)、(32.8±10.3)、(29.1±17.4)ms差异无统计学意义(P>0.05)。(2)血Hcy浓度与静息心率呈正相关(r=0.245,P=0.003),与SDNN、SDNN index、rMSSD、pNN50、HF及LF呈负相关(r<0,P<0.05)。结论 随着Hcy的升高,H型高血压病人的静息心率增加,心率变异性下降,且当血Hcy浓度在15 μmol/L以上时,这种变化更显著。     

The effects of sildenafil on heart rate variability in healthy subjects

The effects of sildenafil on heart rate variability were investigated in 20 healthy male subjects aged 24 (21 to 32) years (median; range). Subjects orally received single 100-mg doses of sildenafil and placebo under randomized double-blind crossover conditions on 2 separate study days. Time domain measures of heart rate variability were assessed under conditions of relaxed rest, metronomic breathing (6 cycles per minute), and bicycle ergometry before administration of sildenafil and placebo as well as 60 minutes afterwards. Sildenafil did not alter heart rate nor heart rate variability to a significant extent (P > 0.05).     

麻黄碱与去氧肾上腺素对胎心率的影响

目的比较麻黄碱与去氧肾上腺素对胎心率的影响。方法择期脊麻下行剖宫产手术的单胎足月妊娠产妇60例均分为两组。Ⅰ组泵注麻黄碱(4mg/ml);Ⅱ组泵注去氧肾上腺素(50μg/ml),调整药物输注速度维持血压接近术前基础值。监测胎儿娩出前胎心率(FHR)和产妇的血压(MAP)、心率(HR)。结果Ⅰ组发生胎儿心动过速18例(60.0%),明显多于Ⅱ组的3例(10.0%)(P<0.05);Ⅰ组产妇术中低血压、高血压和恶心呕吐的发生率高于Ⅱ组(P<0.05)。结论去氧肾上腺素可快速有效地纠正产妇低血压,但不会引起胎心率增快。     

Effect of yoga training on maze learning

The performance in a maze learning task was assessed in adults of either sex (n = 31) before and after 30 days of yoga training and in an age and gender matched control group of subjects who did not receive training in yoga. Subjects were blind folded and used the dominant hand to trace the path in a wooden pencil maze. At each assessment, subjects were given 5 trials, without a gap between them. Performance was based on the time taken to complete the maze and the number of blind alleys taken. The time and error scores of Trial 1 were significantly less after yoga (two-factor ANOVA, Tukey test). Repeating trials significantly decreased time scores at Trial 5 versus Trial 1, for both groups on Day 1 and for the control group on Day 30. Hence the yoga group showed improved performance in maze tracing at retest 30 days later, which may be related to this group being faster learners and also the effect of yoga itself. Yoga training did not influence maze learning, based on the performance in 5 repeat trials.     

Effect of cigarette smoking on fetal breathing movements in normal pregnancies.

In 18 women with uncomplicated pregnancies smoking two cigarettes significantly reduced the proportion of the time that fetal breathing movements were present.     

Effects of clonidine on canine cardiac neuroeffector structures controlling heart rate

1 In intact dogs anaesthetized with pentobarbitone, clonidine (10 μg/kg, i.v.) produced a sustained decrease in heart rate. This effect was significantly smaller in vagotomized dogs in which the sympathetic drive to the heart was either left intact or experimentally created by continuous electrical stimulation of the decentralized cardioaccelerator nerve. In the latter preparation, the negative chronotropic action of clonidine was reversed by an intravenous injection of phentolamine, whereas in the former experimental situation it was antagonized only by an intravenous plus an intravertebral artery injection of phentolamine.

2 In dogs with denervated hearts the tachycardia produced by electrical stimulation of the cardioaccelerator nerve was accompanied by a rise in noradrenaline overflowing into the coronary sinus plasma. Clonidine inhibited both these effects and phentolamine restored them to pre-clonidine levels.

3 Clonidine decreased heart rate in dogs with an intact parasympathetically innervated heart and decentralized stellate ganglia. When the low basal heart rate of this preparation was elevated by electrical stimulation of the cardioaccelerator nerve, clonidine had a negative chronotropic effect, the degree of which was similar to that observed in intact dogs.

4 Clonidine neither modified baseline heart rates of dogs with denervated hearts nor the levels of heart rate which in this preparation were reduced by a sustained electrical stimulation of the right vagus or increased by intravenous infusions of either isoprenaline or noradrenaline.

5 These findings indicate that in the intact dog, bradycardia induced by clonidine resulted both from a reduction of sympathetic drive and from a concomitant increase in parasympathetic tone. The latter action did not occur at the level of cardiac neuroeffector structures since it was observed only in the presence of centrally connected vagal pathways. The inhibition of cardiac sympathetic tone was of both peripheral and central origin. Clonidine, in fact, diminished the quantity of noradrenaline overflowing into the coronary sinus plasma in cardiac denervated dogs with a tachycardia elicited by electrical stimulation of the decentralized cardioaccelerator nerve. This peripheral effect was probably due to an activation of α-adrenoceptors located on sympathetic nerve terminals since it was antagonized by phentolamine. However, in vagotomized dogs (intact sympathetic pathways) intravenous phentolamine failed to antagonize the heart rate effects of clonidine which were abolished by a subsequent injection of phentolamine into the vertebral artery. Thus, the clonidine-induced inhibition of both the peripheral and central sympathetic drive to the heart would appear to be mediated via α-adrenoceptors.